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Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus.

Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Research Abstract Details 

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  • Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Abstract Text:

    yuto uedaYuto Ueda,hidekatsu yokoyamaHidekatsu Yokoyama,akira nakajimaAkira Nakajima,jun tokumaruJun Tokumaru,taku doiTaku Doi,yoshio mitsuyamaYoshio Mitsuyama,

    Kainic acid (KA) induces seizures and degeneration in CA1 of the ventral hippocampus, though its mechanism of action is unknown. We used KA to induce seizures in freely moving rats prepared for in vivo microdialysis with probe placement, and then measured extracellular glutamate with an online fluorometric detector. Generation of free radicals was monitored by electron paramagnetic resonance (EPR) spectroscopy coupled with perfusion of the spin-trapping agent, alpha-(4-pyridyl- N-oxide)- N- tert-butylnitrone (POBN). Regional antioxidant efficacy was measured by observing the eliminating ratio of nitroxide radicals, using 3-carbamoyl-2, 2, 5, 5-tetramethylpyrrolidine-1-oxyl (carbamoyl-PROXYL) applied exogenously from the probe. Increased levels of extracellular glutamate observed at the initiation of KA-induced seizures appear to be associated with generation of lipid free radicals and with a decrease in residual antioxidant effects. These data suggest that collapse of the redox state in the hippocampus, the region most vulnerable to injury from seizure activity, may be critical in the regional injury induced by seizures. Further, we propose that the functional failure of glutamate transporters due to oxidative stress results in high levels of extracellular glutamate during sustained generalized seizures induced with KA.

    Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Publishing Authors By Initials

    y uedaY Ueda,h yokoyamaH Yokoyama,a nakajimaA Nakajima,j tokumaruJ Tokumaru,t doiT Doi,y mitsuyamaY Mitsuyama,

    For similar nervous system diseases: central nervous system diseases: brain diseases: epilepsy: status epilepticus research abstracts see: nervous system diseases: central nervous system diseases: brain diseases: epilepsy: status epilepticus research

    PUBMED ID PMID:

    MEDLINE DATE:

    Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Experimental brain research. Experimentelle Hirnfo

    VOLUME: 147

    Page Numbers: 219-26

    Journal Abbreviation:

    ISSN: 0014-4819

    DAY: 25

    MONTH: 09

    YEAR: 2002

    Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 43312

    Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Keywords Mesh Terms:

    KEYWORDS: Status Epilepticus

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Information

    Substance Name: Glutamic Acid

    Registry Number: 56-86-0

    Grant and Affiliation Information for Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus.

    AFFILIATION: Department of Psychiatry, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan. usan@post1.miyazaki-med.ac.jp

    Country: Germany

    Germany Research PublicationGermany Research Publication

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    ACRONYM:

    MEDLINETA: Exp Brain Res

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